Laterality in Parkinson's disease: A neuropsychological review.

Laterality of motor symptom onset in Parkinson's disease is both well-known and under-appreciated. Treatment of disorders that have asymmetric pathological features, such as stroke and epilepsy, demonstrate the importance of incorporating hemispheric lateralization and specialization into therapy and care planning. These practices could theoretically extend to Parkinson's disease, providing increased diagnostic accuracy and improved treatment outcomes. Additionally, while motor symptoms have generally received the majority of attention, non-motor features (e.g., autonomic dysfunction) also decrease quality of life and are influenced by asymmetrical neurodegeneration. Due to the laterality of cognitive and behavioral processes in the two brain hemispheres, analysis of hemibody side of onset can potentially give insight into expected symptom profile of the patient and allow for increased predictive accuracy of disease progression and outcome, thus opening the door to personalized and improved therapy in treating Parkinson's disease patients. This review discusses motor and non-motor symptoms (namely autonomic, sensory, emotional, and cognitive dysfunction) of Parkinson's disease in respect to hemispheric lateralization from a theoretical perspective in hopes of providing a framework for future research and personalized treatment.

Spreading activation in emotional memory networks and the cumulative effects of somatic markers.

The theory of spreading activation proposes that the activation of a semantic memory node may spread along bidirectional associative links to other related nodes. Although this theory was originally proposed to explain semantic memory networks, a similar process may be said to exist with episodic or emotional memory networks. The Somatic Marker hypothesis proposes that remembering an emotional memory activates the somatic sensations associated with the memory. An integration of these two models suggests that as spreading activation in emotional memory networks increases, a greater number of associated somatic markers would become activated. This process would then result in greater changes in physiological functioning. We sought to investigate this possibility by having subjects recall words associated with sad and happy memories, in addition to a neutral condition. The average ages of the memories and the number of word memories recalled were then correlated with measures of heart rate and skin conductance. The results indicated significant positive correlations between the number of happy word memories and heart rate (r = .384, p = .022) and between the average ages of the sad memories and skin conductance (r = .556, p = .001). Unexpectedly, a significant negative relationship was found between the number of happy word memories and skin conductance (r = -.373, p = .025). The results provide partial support for our hypothesis, indicating that increasing spreading activation in emotional memory networks activates an increasing number of somatic markers and this is then reflected in greater physiological activity at the time of recalling the memories.

Frontal lobe regulation of blood glucose levels: support for the limited capacity model in hostile violence-prone men.

Hostile men have reliably displayed an exaggerated sympathetic stress response across multiple experimental settings, with cardiovascular reactivity for blood pressure and heart rate concurrent with lateralized right frontal lobe stress (Trajanoski et al., in Diabetes Care 19(12):1412-1415, 1996; see Heilman et al., in J Neurol Neurosurg Psychiatry 38(1):69-72, 1975). The current experiment examined frontal lobe regulatory control of glucose in high and low hostile men with concurrent left frontal lobe (Control Oral Word Association Test [verbal]) or right frontal lobe (Ruff Figural Fluency Test [nonverbal]) stress. A significant interaction was found for Group × Condition, F (1,22) = 4.16, p ≤ .05 with glucose levels (mg/dl) of high hostile men significantly elevated as a function of the right frontal stressor (M = 101.37, SD = 13.75) when compared to the verbal stressor (M = 95.79, SD = 11.20). Glucose levels in the low hostile group remained stable for both types of stress. High hostile men made significantly more errors on the right frontal but not the left frontal stressor (M = 17.18, SD = 19.88) when compared to the low hostile men (M = 5.81, SD = 4.33). These findings support our existing frontal capacity model of hostility (Iribarren et al., in J Am Med Assoc 17(19):2546-2551, 2000; McCrimmon et al., in Physiol Behav 67(1):35-39, 1999; Brunner et al., in Diabetes Care 21(4):585-590, 1998), extending the role of the right frontal lobe to regulatory control over glucose mobilization.

Functional cerebral space theory: Towards an integration of theory and mechanisms of left hemineglect, anosognosia, and anosodiaphoria.

BACKGROUND: The current case study presents a 43 year old African American woman admitted to a Tertiary Care Rehabilitation unit at a major medical center for concerns over left-sided anesthesia and weakness. Head scans indicate a right middle cerebral arterial distribution infarct altering blood flow in temporal, parietal, and occipital regions in the right cerebral hemisphere. OBJECTIVE: Physician and therapist reports (i.e., speech and occupational therapists) referred the patient for a neuropsychological evaluation for concerns over the patient's capacity to recognize the severity of her deficits and self-care, with potential rule-outs indicated by the extant literature on right CVA for anosognosia, anosodiaphoria, and left hemibody/hemispace neglect. METHODS: The current case integrates interdisciplinary physician notation, magnetic resonance imaging and magnetic resonance angiogram, observations and reports from speech and occupational therapy, and neuropsychological assessment via standardized tests and neurobehavioral syndrome analysis. RESULTS: Evidence was found for co-occurring syndromes of moderate anosognosia, anosodiaphoria, and left hemibody/hemispatial neglect derived from shared functional cerebral space with overlapping temporal, parietal, and occipital damage. CONCLUSIONS: Clinical implications are discussed, including recommendations for therapy approaches based on functional cerebral space theory that may indicate the use of known techniques (e.g., for left hemibody neglect) that may also have therapeutic implications for treating other, more mercurial co-occurring syndromes of anosognosia and anosodiaphoria.

Administration of exogenous melatonin increases spreading activation in lexical memory networks.

OBJECTIVE: Several studies have examined the effect of exogenous melatonin on memory and cognitive functioning. Many of these investigations have reported improvement in recall and recognition as well as performance on various other indices of neuropsychological functioning. However, there have been no investigations reported that have examined the effects of exogenous melatonin administration on spreading activation in lexical and semantic memory networks. Hence, the purpose of this investigation was to determine the effects of melatonin on spreading activation. METHODS: Participants were randomly assigned to either a 3-mg or 5-mg dose group, and spreading activation was measured both before and after administration. Spreading activation was measured by calculating the average word frequencies for words generated on the controlled oral word association test and the semantic fluency test. RESULTS: A significant main effect for time was found, with the controlled oral word association test average word frequency being significantly higher at baseline than after taking melatonin. Also, a significant group × time interaction was found when using log transformed data. Multiple comparisons indicated that the 3-mg group exhibited significantly greater spreading activation following melatonin than the 5-mg group. The results indicate that melatonin may produce an increase in spreading activation in lexical memory networks. These results potentially provide an explanation for the benefits of melatonin on memory functioning.